Salirasib | Ras inhibitor
NMR (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 5 mg | $35.00 | ||
| 25 mg | $140.00 |
Salirasib (162520-00-5) is a synthetic farnesylcysteine mimetic that inhibits ras proteins1,2 via disruption of interactions between the S-Prenyl moiety of Ras and the membrane anchorage domains3. It has been investigated in the treatment of various cancers.4,5 HCC cells pretreated with salirasib were sensitized to TRAIL-induced apoptosis.6 Salirasib has also been shown to inhibit TRPA1 (EC50 = 1.3 μM).7
References/Citations:
1) Marciano et al. (1995), Farnesyl Derivatives of Rigid Carboxylic Acids – Inhibitors of ras-Dependent Cell Growth; J. Med. Chem., 38 1267
2) Marom et al. (1995), Selective inhibition of Ras-dependent cell growth by farnesylthiosalicylic acid (salirasib) in patients with solid tumors; J. Biol. Chem., 270 22263
3) Haklai et al. (1998), Dislodgement and Accelerated Degradation of Ras; Biochemistry, 37 1306
4) Laheru et al. (2012), Integrated preclinical and clinical development of S-trans,trans-Farnesylthiosalicylic acid (FTS, Salirasib) in pancreatic cancer; Invest .New Drugs, 30 2391
5) Tsimberidou et al. (2010), Phase 1 first-in-human clinical study of S-trans,trans-farnesylthiosalicylic acid (salirasib) in patients with solid tumors; Cancer Chemother. Pharmacol., 65 235
6) Charette et al. (2013), Salirasib sensitizes hepatocarcinoma cells to TRAIL-induced apoptosis through DR5 and survivin-dependent mechanisms; Cell Death and Disease. 4 e471
7) Maher et al. (2008), Activation of TRPA1 by farnesyl thiosalicylic acid; Mol. Pharmacol., 73 1225
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
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Salirasib (162520-00-5) is a synthetic farnesylcysteine mimetic that inhibits ras proteins1,2 via disruption of interactions between the S-Prenyl moiety of Ras and the membrane anchorage domains3. It has been investigated in the treatment of various cancers.4,5 HCC cells pretreated with salirasib were sensitized to TRAIL-induced apoptosis.6 Salirasib has also been shown to inhibit TRPA1 (EC50 = 1.3 μM).7
References/Citations:
1) Marciano et al. (1995), Farnesyl Derivatives of Rigid Carboxylic Acids – Inhibitors of ras-Dependent Cell Growth; J. Med. Chem., 38 1267
2) Marom et al. (1995), Selective inhibition of Ras-dependent cell growth by farnesylthiosalicylic acid (salirasib) in patients with solid tumors; J. Biol. Chem., 270 22263
3) Haklai et al. (1998), Dislodgement and Accelerated Degradation of Ras; Biochemistry, 37 1306
4) Laheru et al. (2012), Integrated preclinical and clinical development of S-trans,trans-Farnesylthiosalicylic acid (FTS, Salirasib) in pancreatic cancer; Invest .New Drugs, 30 2391
5) Tsimberidou et al. (2010), Phase 1 first-in-human clinical study of S-trans,trans-farnesylthiosalicylic acid (salirasib) in patients with solid tumors; Cancer Chemother. Pharmacol., 65 235
6) Charette et al. (2013), Salirasib sensitizes hepatocarcinoma cells to TRAIL-induced apoptosis through DR5 and survivin-dependent mechanisms; Cell Death and Disease. 4 e471
7) Maher et al. (2008), Activation of TRPA1 by farnesyl thiosalicylic acid; Mol. Pharmacol., 73 1225
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